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Evaluation of the serum catalase and myeloperoxidase activities in chronic arsenic-exposed individuals and concomitant cytogenetic damage.评价慢性砷暴露个体的血清过氧化氢酶和髓过氧化物酶活性及伴随的细胞遗传学损伤。
Toxicol Appl Pharmacol. 2010 Nov 15;249(1):47-54. doi: 10.1016/j.taap.2010.08.013. Epub 2010 Aug 20.
2
Changes in serum thioredoxin among individuals chronically exposed to arsenic in drinking water.长期饮用砷污染水人群血清硫氧还蛋白的变化。
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Signal transduction disturbance related to hepatocarcinogenesis in mouse by prolonged exposure to Nanjing drinking water.长期饮用南京自来水导致小鼠肝癌形成过程中的信号转导障碍。
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本文引用的文献

1
Status of groundwater arsenic contamination in the state of West Bengal, India: a 20-year study report.印度西孟加拉邦地下水砷污染状况:一份20年的研究报告。
Mol Nutr Food Res. 2009 May;53(5):542-51. doi: 10.1002/mnfr.200700517.
2
Biomarkers of oxidative stress and damage in human populations exposed to arsenic.暴露于砷的人群中氧化应激和损伤的生物标志物。
Mutat Res. 2009 Mar 31;674(1-2):85-92. doi: 10.1016/j.mrgentox.2008.09.020. Epub 2008 Oct 15.
3
DNA repair deficiency leads to susceptibility to develop arsenic-induced premalignant skin lesions.DNA修复缺陷会导致易患砷诱导的皮肤癌前病变。
Int J Cancer. 2008 Jul 15;123(2):283-287. doi: 10.1002/ijc.23478.
4
Mechanism of erythrocyte death in human population exposed to arsenic through drinking water.通过饮用水接触砷的人群中红细胞死亡的机制。
Toxicol Appl Pharmacol. 2008 Jul 1;230(1):57-66. doi: 10.1016/j.taap.2008.02.003. Epub 2008 Feb 15.
5
Arsenic-induced mitochondrial instability leading to programmed cell death in the exposed individuals.砷诱导的线粒体不稳定导致暴露个体发生程序性细胞死亡。
Toxicology. 2008 Apr 18;246(2-3):101-11. doi: 10.1016/j.tox.2007.12.029. Epub 2008 Jan 12.
6
Vitamin E supplementation protects oxidative stress during arsenic and fluoride antagonism in male mice.补充维生素E可保护雄性小鼠在砷和氟拮抗过程中的氧化应激。
Drug Chem Toxicol. 2007;30(3):263-81. doi: 10.1080/01480540701380075.
7
Insights into the carcinogenic mode of action of arsenic.对砷致癌作用模式的见解。
Toxicol Appl Pharmacol. 2007 Aug 1;222(3):281-8. doi: 10.1016/j.taap.2006.10.006. Epub 2006 Oct 13.
8
8-Oxoguanine DNA glycosylase and MutY homolog are involved in the incision of arsenite-induced DNA adducts.8-氧代鸟嘌呤DNA糖基化酶和MutY同源物参与亚砷酸盐诱导的DNA加合物的切割。
Toxicol Sci. 2007 Feb;95(2):376-82. doi: 10.1093/toxsci/kfl166. Epub 2006 Nov 13.
9
Polymorphism in the ERCC2 codon 751 is associated with arsenic-induced premalignant hyperkeratosis and significant chromosome aberrations.ERCC2基因第751位密码子的多态性与砷诱导的癌前角质化过度及显著的染色体畸变相关。
Carcinogenesis. 2007 Mar;28(3):672-6. doi: 10.1093/carcin/bgl181. Epub 2006 Oct 17.
10
Comparison of health effects between individuals with and without skin lesions in the population exposed to arsenic through drinking water in West Bengal, India.印度西孟加拉邦通过饮用水接触砷的人群中,有皮肤病变者与无皮肤病变者健康影响的比较。
J Expo Sci Environ Epidemiol. 2007 May;17(3):215-23. doi: 10.1038/sj.jes.7500510. Epub 2006 Jul 12.

评价慢性砷暴露个体的血清过氧化氢酶和髓过氧化物酶活性及伴随的细胞遗传学损伤。

Evaluation of the serum catalase and myeloperoxidase activities in chronic arsenic-exposed individuals and concomitant cytogenetic damage.

机构信息

Molecular and Human Genetics Division, Indian Institute of Chemical Biology, Kolkata, India.

出版信息

Toxicol Appl Pharmacol. 2010 Nov 15;249(1):47-54. doi: 10.1016/j.taap.2010.08.013. Epub 2010 Aug 20.

DOI:10.1016/j.taap.2010.08.013
PMID:20732340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3457024/
Abstract

Chronic arsenic exposure through contaminated drinking water is a major environmental health issue. Chronic arsenic exposure is known to exert its toxic effects by a variety of mechanisms, of which generation of reactive oxygen species (ROS) is one of the most important. A high level of ROS, in turn, leads to DNA damage that might ultimately culminate in cancer. In order to keep the level of ROS in balance, an array of enzymes is present, of which catalase (CAT) and myeloperoxidase (MPO) are important members. Hence, in this study, we determined the activities of these two enzymes in the sera and chromosomal aberrations (CA) in peripheral blood lymphocytes in individuals exposed and unexposed to arsenic in drinking water. Arsenic in drinking water and in urine was used as a measure of exposure. Our results show that individuals chronically exposed to arsenic have significantly higher CAT and MPO activities and higher incidence of CA. We found moderate positive correlations between CAT and MPO activities, induction of CA and arsenic in urine and water. These results indicate that chronic arsenic exposure causes higher CAT and MPO activities in serum that correlates with induction of genetic damage. We conclude that the serum levels of these enzymes might be used as biomarkers of early arsenic exposure induced disease much before the classical dermatological symptoms of arsenicosis begin to appear.

摘要

慢性砷暴露通过污染饮用水是一个主要的环境健康问题。慢性砷暴露已知通过多种机制发挥其毒性作用,其中生成活性氧物种 (ROS) 是最重要的机制之一。高水平的 ROS 反过来又导致 DNA 损伤,最终可能导致癌症。为了保持 ROS 的水平平衡,存在一系列的酶,其中过氧化氢酶 (CAT) 和髓过氧化物酶 (MPO) 是重要的成员。因此,在这项研究中,我们测定了暴露和未暴露于饮用水砷的个体血清中的这两种酶的活性和外周血淋巴细胞中的染色体畸变 (CA)。饮用水和尿液中的砷被用作暴露的衡量标准。我们的结果表明,慢性砷暴露的个体血清中的 CAT 和 MPO 活性显著升高,CA 的发生率也更高。我们发现 CAT 和 MPO 活性、CA 诱导与尿液和水中的砷之间存在中度正相关。这些结果表明,慢性砷暴露导致血清中 CAT 和 MPO 活性升高,这与遗传损伤的诱导有关。我们得出结论,这些酶的血清水平可能被用作早期砷暴露诱导疾病的生物标志物,远早于砷中毒的典型皮肤病症状开始出现。